Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the possible route of transmission of Helicobacter pylori, stomach biopsies and dental plaques were cultured from patients with dyspeptic symptoms who underwent endoscopy. A total of 31 patients were examined. Twenty patients out of thirty one (64%) were H. pylori positive in gastric biopsy. Among the microorganisms isolated in dental plaque only one sample (corresponding to a patients with duodenal ulcer H. pylori positive) showed colonies morphologically and biochemically compatible with H. pylori. Proteic patterns of whole cells and restriction endonuclease analysis with Hind III and Hae III endonucleases of DNA extracted from the strain subcultured from a stomach biopsy and from dental plaque of the same patient indicated that both sites were infected with the same strain of H. pylori.
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PMID:Microbiological evidence of Helicobacter pylori from dental plaque in dyspeptic patients. 760 46

Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) may be involved in the pathogenesis of peptic ulcers through suppression of fibrinolysis. This study was designed to investigate associations of t-PA and PAI-1 genes with clinical features of the patients with bleeding gastric ulcers. Eighty-four patients with peptic ulcers and 100 controls were studied between January 1998 and April 2000. We used polymerase chain reaction and endonuclease digestion to genotype for 4G/5G polymorphism in the promoter region of the PAI-1 gene and the Alurepeat insertion/deletion (I/D) polymorphism in intron h of the t-PA gene. Various clinical features, including lesion site, bleeding event, recurrence of ulcer, and rebleeding, were assessed using a multiple logistic regression model. The genotype distributions of both the t-PA and PAI-1 genes did not differ between the patient and control groups. The occurrence of the I/D or D/D genotype of t-PA was significantly higher in cases of duodenal ulcer (adjusted OR=4.39, 95% CI=1.12-17.21). When a dominant effect (i.e., 4G/4G or 4G/5G versus 5G/5G) of the 4G allele was assumed, the PAI-1 4G/4G genotype was independently associated with rebleeding after hemostasis (adjusted OR=5.07, 95% CI=1.03-24.87). Our data suggest that t-PA gene polymorphism is associated with duodenal ulcers, and that the PAI-1 gene may be a risk factor leading to recurrent bleeding after initial hemostasis.
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PMID:Tissue plasminogen activator and plasminogen activator inhibitor type 1 gene polymorphism in patients with gastric ulcer complicated with bleeding. 1258 88